Abstract
B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.
| Original language | English |
|---|---|
| Pages (from-to) | 227-237 |
| Number of pages | 11 |
| Journal | Cancer letters |
| Volume | 266 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2008 Aug 8 |
| Externally published | Yes |
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Keywords
- Apoptosis
- B cell
- B7-H4
- EBV
- Fas
- FasL
ASJC Scopus subject areas
- Oncology
- Cancer Research
Cite this
B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation. / Song, Hyunkeun; Park, Gabin; Kim, Yeong Seok; Hur, Indo; Kim, Hyunjin; Ryu, Jeoung Whan; Lee, Hyun Kyung; Cho, Dae Ho; Choi, In Hak; Lee, Wang Jae; Hur, Dae Young.
In: Cancer letters, Vol. 266, No. 2, 08.08.2008, p. 227-237.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation
AU - Song, Hyunkeun
AU - Park, Gabin
AU - Kim, Yeong Seok
AU - Hur, Indo
AU - Kim, Hyunjin
AU - Ryu, Jeoung Whan
AU - Lee, Hyun Kyung
AU - Cho, Dae Ho
AU - Choi, In Hak
AU - Lee, Wang Jae
AU - Hur, Dae Young
PY - 2008/8/8
Y1 - 2008/8/8
N2 - B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.
AB - B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.
KW - Apoptosis
KW - B cell
KW - B7-H4
KW - EBV
KW - Fas
KW - FasL
UR - http://www.scopus.com/inward/record.url?scp=45049087541&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=45049087541&partnerID=8YFLogxK
U2 - 10.1016/j.canlet.2008.02.067
DO - 10.1016/j.canlet.2008.02.067
M3 - Article
C2 - 18417276
AN - SCOPUS:45049087541
VL - 266
SP - 227
EP - 237
JO - Cancer Letters
JF - Cancer Letters
SN - 0304-3835
IS - 2
ER -